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Proprotein Convertase Subtilisin/Kexin Type 9 [PDF]
Chiara Macchi +2 more
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Proprotein convertase subtilisin/kexin type 9 inhibition
Current Opinion in Lipidology, 2012There are now ample data that demonstrate that inhibition of PCSK9 (proprotein convertase subtilisin/kexin type 9) can safely lower LDL cholesterol synergistically with statins. Considering that PCSK9 was first identified less than a decade ago, the last few years have shown rapid and remarkable advancements in our understanding and knowledge of the ...
David A, Marais +4 more
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Natural Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: A Review
Combinatorial Chemistry & High Throughput Screening, 2023Abstract: PCSK9 (proprotein convertase subtilisin/kexin type 9) is an enzyme that helps to reduce cardiovascular events. This clinical result is attributable primarily to the crucial involvement of PCSK9 in regulating the low-density lipoprotein cholesterol level.
Sonia Singh +4 more
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Proprotein convertase subtilisin/kexin type 9
Current Opinion in Cardiology, 2018This review describes the pivotal role of genetic insights and technologies in the discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9) and the rapid development of PCSK9 inhibitors - a revolutionary new class of lipid-lowering agents.PCSK9 was discovered as a the third gene implicated in familial hypercholesterolemia. Population genetics
Robert M, Stoekenbroek +1 more
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Proprotein Convertase Subtilisin/Kexin-Type 9 and Lipid Metabolism
2020Plasma levels of cholesterol, especially low-density lipoprotein cholesterol (LDL-C), are positively correlated with the risk of cardiovascular disease. Buildup of LDL in the intima promotes the formation of foam cells and consequently initiates atherosclerosis, one of the main underlying causes of cardiovascular disease. Hepatic LDL receptor (LDLR) is
Shoudong, Guo +3 more
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Potential of Proprotein Convertase Subtilisin/Kexin Type 9 Based Therapeutics
Current Atherosclerosis Reports, 2013The link between proprotein convertase subtilisin/kexin type 9 (PCSK9) and cholesterol metabolism was established only in 2003 when genetic mapping and positional cloning in patients with autosomal dominant hypercholesterolemia in which linkage to the loci coding for the LDL receptor and apolipoprotein B had been excluded identified the genetic defect ...
Evan A, Stein, Gary D, Swergold
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Proprotein Convertase Subtilisin/kexin type 9 Inhibition in Cardiovascular Prevention
Current Pharmaceutical Design, 2018Elevated levels of Low Density Lipoprotein cholesterol (LDL-C) are directly associated with increased risk for atherosclerotic cardiovascular and cerebrovascular events. Statins have been used to control serum LDLC and this has translated into reduction in cardiovascular and cerebrovascular events.
Ali, Ali +2 more
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Identification of Novel cDNAs Encoding Human Kexin-Like Protease, PACE4 Isoforms
Biochemical and Biophysical Research Communications, 1994PACE4 has been identified as a second human subtilisin-like protease by Keifer et al. [DNA and Cell Biology (1991) 10, 757-769]. In this study, we isolated two novel cDNAs coding for PACE4 isoforms (PACE4C and PACE4D) from a human placenta cDNA library.
A, Tsuji +6 more
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Proprotein convertase subtilisin/kexin type 9 related familial hypercholesterolaemia
The British Journal of Diabetes & Vascular Disease, 2012Gain-of-function proprotein convertase subtilisin/kexin type 9 (PCSK9) mutations are an uncommon cause of familial hypercholesterolaemia (FH) with a reported frequency of less than 2% in patients with FH in the United Kingdom. We have found a high prevalence of this genotype in our patients with FH in northwest England.
Sally L Hanton, Charles Van Heyningen
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A Novel Splicing Variant of Proprotein Convertase Subtilisin/Kexin Type 9
DNA and Cell Biology, 2008Proprotein convertase subtilisin/kexin type 9 (PCSK9) is the most recently identified member of the proprotein convertase family. Genetic and cell biology studies have suggested a critical role of PCSK9 in regulating low-density lipoprotein receptor (LDLR) protein levels and thus modulating plasma LDL cholesterol. Recent data on the molecular basis for
Robert J, Schmidt +13 more
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